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Art ID :258559(Ay)A NEW LABDANE DITERPENOID FROM SCOPARIA DULCIS IMPROVING PANCREATIC FUNCTION AGAINST ISLETS CELL APOPTOTIC BY BAX/BCL-2/CASPASE-3 PATHWAY.

Journal of Ethnopharmacology
2024
322
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1. Lin Dong, 3. Mimi Chen, 1. Zibao Huang, 1. Yinfeng Tan, 1,2. Caiyun Zhang, 3. Shouwen Zhang, 1. Yong Zhang, 1,2. Xiaopo Zhang.
1. Key Laboratory of Tropical Translational Medicine of Ministry of Education, Hainan Key Laboratory for Research and Development of Tropical Herbs, School of Pharmacy, Hainan Medical University, Haikou, 571199, China. 2. Research Center for Drug Safety Evaluation of Hainan Province, Hainan Medical University, Haikou, 571101, China. 3. Research Center for Traditional Chinese Medicine Resources and Ethnic Minority Medicine, Jiangxi University of Chinese Medicine, Nanchang, 330004, China.
1. Yong Zhang, Key Laboratory of Tropical Translational Medicine of Ministry of Education, Hainan Key Laboratory for Research and Development of Tropical Herbs, School of Pharmacy, Hainan Medical University, Haikou, 571199, China. Email: 935150242@qq.com; 2. Xiaopo Zhang, Key Laboratory of Tropical Translational Medicine of Ministry of Education, Hainan Key Laboratory for Research and Development of Tropical Herbs, School of Pharmacy, Hainan Medical University, Haikou, 571199, China. Email: z_xp1412@163.com
ARP_AYU030874
JOURNAL ARTICLE
PRECLINICAL RESEARCH
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Abstract/ Summary/ Synopsis/ Outline:

Ethnopharmacological relevance: Scoparia dulcis has been identified as a significant ethnopharmacological substance in the Li, Zhuang, and Dai ethnic groups of China. Traditional medicine use S. dulcis to treat numerous illnesses, most notably diabetes. The considerable antidiabetic properties of this herbal remedy have been established by several clinical investigations and animal experiments. The islet is the intended target of S. dulcis, although the cause of its activity and mechanism for diabetes treatment is unclear. The diterpenoids from S. dulcis have been shown in the literature to have significant hypoglycemic efficacy and to protect islet cells in vitro. Diterpenoids may be the components of this herbal remedy that preserve islets, but further research is needed. Aim of the study: This study was projected to investigate the new diterpenoid scoparicol E from S. dulcis and examined its islet-protective effect and the potential mechanism both in vitro and in vivo. Methods: The structure of the novel diterpenoid scoparicol E was clarified by employing a wide range of spectroscopic methods. Using CCK-8 tests, cytotoxicity and antiapoptotic activity of scoparicol E were detected. Serum biochemical analysis and pathologic examination were performed to study the protective effect of scoparicol E against islet damage. The specific mechanism of action of scoparicol E was investigated through the mitochondrial membrane potential, Annexin V-FITC flow cytometry, and western blotting. Results: Scoparicol E reduced MLD-STZ-induced hyperglycemia in mice and increased insulin and islet apoptosis. Scoparicol E effectively suppressed the Bax/Bcl-2/Caspase-3 pathway, according to the in vivo western blot investigation. Scoparicol E showed significant antiapoptotic action in vitro. We also showed that scoparicol E might prevent islet cells from dying by inhibiting the Bax/Bcl-2/Caspase-3 pathway. The Annexin V-FITC flow cytometry results revealed that MIN6 cell apoptosis was considerably decreased following scoparicol E intervention, showing anti-islet cell apoptosis action. Furthermore, the Caspase-3-mediated apoptosis pathway depends on cytochrome c and the potential of the mitochondrial membrane. Scoparicol E prevented the release of cytochrome c, restored the mitochondrial membrane potential, and prevented MIN6 cell apoptosis. Conclusion: We demonstrated the new diterpenoid scoparicol E could protect islet cells apoptosis by modulating the Bax/Bcl-2/Caspase-3 pathway.
Scoparia dulcis , apoptosis , scoparicol E , Bax/Bcl-2/Caspase-3 pathway
https://www.sciencedirect.com/science/article/abs/pii/S0378874123014411
10.1016/j.jep.2023.117571
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Acknowledgment

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